Endothelial and Inflammation Biomarker Profiles at Diagnosis Reflecting Clinical Heterogeneity and Serving as a Prognostic Tool for Treatment Response in Two Independent Cohorts of Patients With Juvenile Dermatomyositis

Juvenile dermatomyositis (DM) is a heterogeneous systemic immune‐mediated vasculopathy. This study was undertaken to 1) identify inflammation/endothelial dysfunction–related biomarker profiles reflecting disease severity at diagnosis, and 2) establish whether such biomarker profiles could be used for predicting the response to treatment in patients with juvenile DM.

[1]  C. Minetti,et al.  Muscle Expression of Type I and Type II Interferons Is Increased in Juvenile Dermatomyositis and Related to Clinical and Histologic Features , 2019, Arthritis & rheumatology.

[2]  S. Kamphuis,et al.  Galectin‐9 and CXCL10 as Biomarkers for Disease Activity in Juvenile Dermatomyositis: A Longitudinal Cohort Study and Multicohort Validation , 2019, Arthritis & rheumatology.

[3]  T. Jacques,et al.  Expression of myxovirus‐resistance protein A: a possible marker of muscle disease activity and autoantibody specificities in juvenile dermatomyositis , 2018, Neuropathology and applied neurobiology.

[4]  L. Wedderburn,et al.  Systemic and Tissue Inflammation in Juvenile Dermatomyositis: From Pathogenesis to the Quest for Monitoring Tools , 2018, Front. Immunol..

[5]  Takuya Inoue,et al.  The relationship between type 1 IFN and vasculopathy in anti-MDA5 antibody-positive dermatomyositis patients. , 2018, Rheumatology.

[6]  K. Rostásy,et al.  Pattern of myogenesis and vascular repair in early and advanced lesions of juvenile dermatomyositis , 2018, Neuromuscular Disorders.

[7]  C. Papadopoulou,et al.  The Vasculopathy of Juvenile Dermatomyositis , 2018, Front. Pediatr..

[8]  L. L. van den Hoogen,et al.  Galectin-9 is an easy to measure biomarker for the interferon signature in systemic lupus erythematosus and antiphospholipid syndrome , 2018, Annals of the rheumatic diseases.

[9]  W. Stenzel,et al.  JAK inhibitor improves type I interferon induced damage: proof of concept in dermatomyositis , 2018, Brain : a journal of neurology.

[10]  C. Bodemer,et al.  Myogenic Progenitor Cells Exhibit Type I Interferon–Driven Proangiogenic Properties and Molecular Signature During Juvenile Dermatomyositis , 2018, Arthritis & rheumatology.

[11]  G. Shaddick,et al.  Autoantibodies in juvenile-onset myositis: Their diagnostic value and associated clinical phenotype in a large UK cohort , 2017, Journal of autoimmunity.

[12]  F. Rieux-Laucat,et al.  Detection of interferon alpha protein reveals differential levels and cellular sources in disease , 2017, The Journal of experimental medicine.

[13]  N. Wulffraat,et al.  Consensus-based recommendations for the management of juvenile dermatomyositis , 2016, Annals of the rheumatic diseases.

[14]  C. Bodemer,et al.  Assessment of Type I Interferon Signaling in Pediatric Inflammatory Disease , 2016, Journal of Clinical Immunology.

[15]  M. De Iorio,et al.  Comparison of the Utility and Validity of Three Scoring Tools to Measure Skin Involvement in Patients With Juvenile Dermatomyositis , 2016, Arthritis care & research.

[16]  C. Bodemer,et al.  Vasculopathy-related clinical and pathological features are associated with severe juvenile dermatomyositis. , 2015, Rheumatology.

[17]  J. Gottenberg,et al.  Incidence and prevalence of inflammatory myopathies: a systematic review. , 2015, Rheumatology.

[18]  T. Bowden,et al.  Timing of Galectin-1 Exposure Differentially Modulates Nipah Virus Entry and Syncytium Formation in Endothelial Cells , 2014, Journal of Virology.

[19]  B. Prakken,et al.  Correlation of CXCL10, Tumor Necrosis Factor Receptor Type II, and Galectin 9 With Disease Activity in Juvenile Dermatomyositis , 2014, Arthritis & rheumatology.

[20]  E. Ferrannini,et al.  Chemokine (C-X-C motif) ligand (CXCL)10 in autoimmune diseases. , 2014, Autoimmunity reviews.

[21]  M. Rebelatto,et al.  Suppression of soluble T cell-associated proteins by an anti-interferon-α monoclonal antibody in adult patients with dermatomyositis or polymyositis , 2013, Rheumatology.

[22]  S. Greenberg,et al.  A phase 1b clinical trial evaluating sifalimumab, an anti-IFN-α monoclonal antibody, shows target neutralisation of a type I IFN signature in blood of dermatomyositis and polymyositis patients , 2013, Annals of the rheumatic diseases.

[23]  E. Tønnesen,et al.  Soluble Adhesion Molecules Correlate with Surface Expression in an In Vitro Model of Endothelial Activation , 2013, Basic & clinical pharmacology & toxicology.

[24]  Chiang-Ching Huang,et al.  Lack of Achievement of a Full Score on the Childhood Myositis Assessment Scale by Healthy Four‐Year‐Olds and Those Recovering From Juvenile Dermatomyositis , 2013, Arthritis care & research.

[25]  J. Malley,et al.  The Clinical Phenotypes of the Juvenile Idiopathic Inflammatory Myopathies , 2013, Medicine.

[26]  S. Amin,et al.  Changes in novel biomarkers of disease activity in juvenile and adult dermatomyositis are sensitive biomarkers of disease course. , 2012, Arthritis and rheumatism.

[27]  S. Sredni,et al.  Increased expression of vascular cell adhesion molecule 1 in muscle biopsy samples from juvenile dermatomyositis patients with short duration of untreated disease is regulated by miR-126. , 2012, Arthritis and rheumatism.

[28]  R. Schneider,et al.  Nailfold capillary density is importantly associated over time with muscle and skin disease activity in juvenile dermatomyositis. , 2011, Rheumatology.

[29]  S. Stowell,et al.  Degeneration of dystrophic or injured skeletal muscles induces high expression of Galectin-1. , 2008, Glycobiology.

[30]  I. Lundberg,et al.  Vascular endothelial growth factor is highly expressed in muscle tissue of patients with polymyositis and patients with dermatomyositis. , 2008, Arthritis and rheumatism.

[31]  M. Perretti,et al.  Inhibitory control of endothelial galectin‐1 on in vitro and in vivo lymphocyte trafficking , 2008, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[32]  P. Lachenbruch,et al.  Preliminary validation and clinical meaning of the Cutaneous Assessment Tool in juvenile dermatomyositis. , 2008, Arthritis and rheumatism.

[33]  A. Paller,et al.  Persistent association of nailfold capillaroscopy changes and skin involvement over thirty-six months with duration of untreated disease in patients with juvenile dermatomyositis. , 2008, Arthritis and rheumatism.

[34]  L. Pachman,et al.  MxA gene expression in juvenile dermatomyositis peripheral blood mononuclear cells: association with muscle involvement. , 2006, Clinical immunology.

[35]  D. Watt,et al.  Galectin‐1 Induces Skeletal Muscle Differentiation in Human Fetal Mesenchymal Stem Cells and Increases Muscle Regeneration , 2006, Stem cells.

[36]  L. Baum,et al.  Endothelial cell expression of galectin-1 induced by prostate cancer cells inhibits T-cell transendothelial migration , 2006, Laboratory Investigation.

[37]  T. Libermann,et al.  Soluble endoglin contributes to the pathogenesis of preeclampsia , 2006, Nature Medicine.

[38]  K. Bove,et al.  What more can we learn from muscle histopathology in children with dermatomyositis/polymyositis? , 2006, Clinical and experimental rheumatology.

[39]  E. Hoffman,et al.  Journal of Autoimmune Diseases BioMed Central , 2006 .

[40]  K. Stringer,et al.  Association between lack of angiogenic response in muscle tissue and high expression of angiostatic ELR-negative CXC chemokines in patients with juvenile dermatomyositis: possible link to vasculopathy. , 2005, Arthritis and rheumatism.

[41]  W. Kuis,et al.  Improved multiplex immunoassay performance in human plasma and synovial fluid following removal of interfering heterophilic antibodies. , 2005, Journal of immunological methods.

[42]  Y. Konttinen,et al.  Disease-associated increased HIF-1, αvβ3 integrin, and Flt-1 do not suffice to compensate the damage-inducing loss of blood vessels in inflammatory myopathies , 2004, Rheumatology International.

[43]  R. Bode,et al.  Disease activity score for children with juvenile dermatomyositis: reliability and validity evidence. , 2003, Arthritis and rheumatism.

[44]  L. Pachman,et al.  Increased plasma thrombospondin-1 (TSP-1) levels are associated with the TNF alpha-308A allele in children with juvenile dermatomyositis. , 2002, Clinical immunology.

[45]  S. Marie,et al.  Immunohistological analysis of CD59 and membrane attack complex of complement in muscle in juvenile dermatomyositis. , 2002, The Journal of rheumatology.

[46]  O. Volpert,et al.  Signals leading to apoptosis-dependent inhibition of neovascularization by thrombospondin-1 , 2000, Nature Medicine.

[47]  P. Lachenbruch,et al.  Development of validated disease activity and damage indices for the juvenile idiopathic inflammatory myopathies. I. Physician, parent, and patient global assessments , 1997 .

[48]  J. Mendell,et al.  Microvascular deposition of complement membrane attack complex in dermatomyositis. , 1986, The New England journal of medicine.

[49]  A. Bohan,et al.  Polymyositis and dermatomyositis (second of two parts). , 1975, The New England journal of medicine.

[50]  A. Bohan,et al.  Polymyositis and dermatomyositis (second of two parts). , 1975 .